HIV e cérebro: do comprometimento neurocognitivo à encefalite por linfócitos T CD8+: relato de caso e revisão de literatura

Abstract

The introduction of Combination Antiretroviral Therapy (cART) dramatically reduced opportunistic infections affecting the central nervous system (CNS), thereby reshaping the landscape of HIV-related neurological disorders. With this epidemiological shift, HIV-Associated Neurocognitive Disorder (HAND) has become increasingly prevalent, ranging from Asymptomatic Neurocognitive Impairment to Mild Neurocognitive Disorder and HIV Associated Dementia. These conditions arise from persistent neuroinflammation and residual viral replication within the CNS, even under effective cART. Immune reconstitution induced by cART has also been accompanied by the emergence of inflammatory complications such as Immune Reconstitution Inflammatory Syndrome (IRIS). Within this context of immune dysregulation, CD8+ T-cell Encephalitis (CD8E) has been recognized as a rare and recently described entity, characterized by exuberant infiltration of CD8+ T lymphocytes within the brain parenchyma and vasculature, frequently associated with cerebrospinal fluid (CSF) viral escape. From a pathophysiological perspective, HIV enters the CNS early via infected monocytes, leading to chronic neuroinflammation driven by microglia and macrophages. In CD8E, however, the pathological pattern diverges from classical HIV encephalitis due to the absence of multinucleated giant cells and minimal p24 expression, with CD8-mediated cytotoxicity predominating. Diagnosis relies on the combination of clinical presentation, neuroimaging findings — typically diffuse white-matter hyperintensities and perivascular enhancement — and CSF analysis. Although definitive confirmation is histopathological, treatment must be initiated promptly with corticosteroid immunosuppression and optimization of cART.The case presented involves a 24-year-old patient with poor treatment adherence who developed a subacute neurological syndrome characterized by psychomotor slowing, tremor, and cognitive impairment. Brain MRI showed diffuse T2/FLAIR white-matter hyperintensities, while CSF analysis revealed marked lymphocytic pleocytosis with CD8+ predominance and significant dissociation between plasma and CSF viral loads. High-dose methylprednisolone therapy led to clinical improvement, although the patient experienced a relapse two years later, again associated with CNS viral escape. This study aims to broaden the recognition of HIV-related CNS manifestations, emphasizing CD8E within the spectrum of HIV-associated encephalitides, particularly in unexplained subacute neurological presentations. By integrating clinical, laboratory, and radiological findings, it highlights the need to develop diagnostic criteria that enable early identification and management of this rare condition, reducing reliance on brain biopsy — an especially relevant consideration in resource-limited settings.